Castling, a novel therapeutic concept for rewiring pathological gene-expression networks, enabled by the TRIPLE technology
Antony, D.; Roman Azcona, M. S.; Kalinski, H.; Pultar, M.; Adamsky, S.; Nachum, S. A.; Shalom, E.; Rhiel, M.; Tsouris, A.; Diendorfer, A.; Andrieux, G.; Boerries, M.; Hackl, M.; Cornu, T. I.; Zurr, D.; Cathomen, T.; Feinstein, E.; Mussolino, C.
Show abstract
Pathological conditions often arise from dysregulation of complex gene networks, with microRNAs (miRNAs) acting as central modulators. Disease progression is frequently characterized by upregulation of "disease-promoting" miRNA, suppressing beneficial pathways, and concomitant downregulation of "protective/therapeutic" miRNAs, normally restraining pathological programs. Since individual miRNAs coordinately regulate multiple genes, their manipulation represents powerful therapeutic intervention, yet synthetic or ectopically overexpressed miRNA mimics or inhibitors may perturb physiological miRNA processing and/or cause off-target effects. We hypothesized that pathological gene regulatory imbalances could instead be corrected by rewiring endogenous miRNA regulation. Specifically, by placing downregulated "protective/therapeutic" miRNAs under the control of promoters activated in pathology, and driving overexpression of "disease-promoting" miRNAs, thereby disabling the pathogenic program while inducing the therapeutic one in a single editing event. We termed this concept castling, after the chess move. For effective implementation of castling, we developed TRIPLE (Targeted Replacement Induced by Persistent Locus Editing), a novel genome-editing procedure enhancing homology-directed repair through sequential cleavage. As proof of concept, we castled miRNAs inversely regulated during onset of CAR T cell dysfunction in a model of chronic antigen stimulation. Castled CAR T cells exhibited a delayed dysfunction enabled by up- and downregulation of relevant gene subsets.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Loss of DHX36/G4R1, a G4 resolvase, drives genome instability and regulates innate immune gene expression in cancer cells 95%
- Deep and accurate detection of m6A RNA modifications using miCLIP2 and m6Aboost machine learning 95%
- Telomemore enables single-cell analysis of cell cycle and chromatin condensation 95%
Similar papers in this journal
- Simultaneous inhibition of DNA-PK and Pol{Theta} improves integration efficiency and precision of genome editing 96%
- SLE non-coding Genetic Risk Variant Determines the Epigenetic Dysfunction of an Immune Cell Specific Enhancer that Controls Disease-critical microRNA Expression 95%
- EZH2 mutations in follicular lymphoma distort H3K27me3 profiles and alter transcriptional responses to PRC2 inhibition 95%
Similar papers in this journal
Similar papers in this journal
- TET2 regulates early and late transitions in exhausted CD8+ T-cell differentiation and limits CAR T-cell function 96%
- HIRA loss transforms FH-deficient cells 95%
- Notch signaling blockade links transcriptome heterogeneity in quiescent neural stem cells with their reactivation routes and potential 95%
Similar papers in this journal
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.